Cytomegalovirus infection increases development of atherosclerosis in Apolipoprotein-E knockout mice
Cytomegalovirus infection increases development of atherosclerosis in Apolipoprotein-E knockout mice
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DOI：
10.1016/s0021-9150(00)00608-0
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发表时间：
2001-05-01
期刊：
影响因子：
5.3
通讯作者：
Epstein, SE
中科院分区：
文献类型：
--
作者：
Hsich, E;Zhou, YF;Epstein, SE
巨细胞病毒（CMV）感染与冠状动脉疾病有关，但尚不清楚该病毒是否会对动脉粥样硬化的形成有因果关系。为了确定该病毒是否具有这种能力，我们用鼠巨细胞病毒感染易患动脉粥样硬化的小鼠品系（C57BL/6J apoE - / -）。在14日龄时，30只小鼠腹腔内接种巨细胞病毒（30000空斑形成单位），30只接受无病毒培养基。在13周和16周时，测量主动脉窦横断面的动脉粥样硬化病变大小。感染未改变血浆胆固醇、甘油三酯和高密度脂蛋白（HDL）水平，然而，感染后4周，干扰素 - γ水平升高（感染组与对照组：156 ± 49比50 ± 22皮克/毫升，P = 0.04）。感染后13周，病变大小无差异。然而，到16周时，巨细胞病毒感染小鼠的平均主动脉窦病变面积（平方毫米×10³ ±标准误；N = 75）显著大于未感染小鼠（74 ± 6比57 ± 6，P = 0.04）。巨细胞病毒在雌性小鼠中导致病变大小增加最多（34%）（103 ± 9比77 ± 10；P = 0.05，N = 35）。这些结果提供了更多证据，表明巨细胞病毒是动脉粥样硬化的病因，至少在动物模型中是如此。（C）2001爱思唯尔科学爱尔兰有限公司。保留所有权利。
Cytomegalovirus (CMV) infection has been associated with coronary artery disease. but it is unknown whether the virus can causally contribute to atherogenesis. To determine whether the virus has this capacity. we infected an atherosclerotic-prone mouse strain (C57BL/6J apoE-/-) with murine CMV. At 14 days of age, 30 mice received CMV (30 000 pfu) ip and 30 received virus free media. At 13 and 16 weeks atherosclerotic lesion size was measured from aortic sinus cross-sections. Infection did not alter plasma levels of cholesterol, triglycerides, and high density lipoprotein (HDL), however, 4 weeks after infection IFN gamma levels were elevated (infection vs control: 156 +/- 49 vs 50 +/- 22 pg/ml, P = 0.04). No differences in lesion size were present at 13 weeks post infection. However. by 16 weeks mean aortic sinus lesion area (mm(2) x 10(3) +/- SEM; N = 75) in the CMV-infected mice was significantly greater than in uninfected mice (74 +/- 6 vs 57 +/- 6, P = 0.04). CMV caused the greatest increase (34%) in lesion size in females (103 +/- 9 vs 77 +/- 10; P = 0.05, N = 35). These results provide additional evidence implicating CMV as a causal agent of atherosclerosis, at least in an animal model. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.